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首页> 外文期刊>Journal of Cellular Physiology >Protease activated receptor-1, PAR1, promotes placenta trophoblast invasion and beta-catenin stabilization.
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Protease activated receptor-1, PAR1, promotes placenta trophoblast invasion and beta-catenin stabilization.

机译：蛋白酶激活receptor-1 PAR1,促进胎盘滋养层入侵和β-连环蛋白稳定。

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Despite extensive efforts toward elucidation of the molecular pathway controlling cytotrophoblast (CTB) invasion to the uterine decidua, it remains poorly defined. There are striking similarities between tumor cell invasion and cytotrophoblast implantation to the deciduas whereby the role of Protease Activated Receptors (PARs) and wnt signaling is well recognized. We examine here consequences of modulation of PAR1 and PAR2 expression and function on CTB invasion and beta-catenin stabilization. Toward this end, we utilized a model system of extravillous trophoblast (EVT) organ culture and various placenta cell lines (e.g., JAR and HTR-8/Svneo). Activation of PAR1 induces EVT invasion while hPar1-SiRNA and PAR1 antagonist SCH79797--effectively inhibited it. In parallel, the Wnt inhibitor Dickkopf-1 (Dkk1) similarly inhibited it. Nuclear localization of beta-catenin is seen only after PAR1 activation, and is markedly reduced following the application of hPar1-SiRNA construct and PAR1 antagonist in CTBs. In contrast, PAR2 elicited a low cytoplasmic beta-catenin level as also proliferation and invasion. In the non-activated CTBs in-comparison, beta-catenin appeared limited to the membrane pools. Concomitantly, a temporal regulated pattern of Wnt-4, 5a, 7b, 10a, 10b expression is seen along PAR1 appearance. Enforced expression of Wnt antagonists, Secreted Frizzled Related Proteins; SFRP2 & 5; into HTR-8/Svneo, resulted with a markedly reduced nuclear beta-catenin levels, similar to the effect obtained by hPar1-SiRNA treatment. Identification of PAR1 downstream target/s may nonetheless contribute to the formation of a future platform system for eliciting a firm placenta-uterus interactions and to the definition of late pregnancy outcomes.
机译：尽管广泛努力说明分子通路控制细胞滋养层(施)入侵子宫蜕膜,它仍然存在差的定义。肿瘤细胞入侵和细胞滋养层之间植入的蜕膜的作用蛋白酶激活受体(PARs)和wnt信号很容易被识别。调制PAR1和PAR2的后果在所有入侵和表达和功能β-连环蛋白稳定。利用extravillous的模型系统滋养层(EVT)文化和各种器官胎盘细胞系(如JAR和HTR-8 / Svneo)。激活PAR1诱发EVT入侵SCH79797——有效地抑制它。Wnt抑制剂Dickkopf-1 (Dkk1)类似抑制它。β-连环蛋白被认为只有PAR1激活后,和明显减少应用程序hPar1-SiRNA构造和PAR1拮抗剂施莱。细胞质β-连环蛋白水平核扩散和入侵。施相比,β-连环蛋白似乎有限膜池。监管模式Wnt-4 5 7 b, 10 a, b表达式是沿着PAR1外观。执行的Wnt拮抗剂的表达,分泌卷曲的相关蛋白;HTR-8 / Svneo,明显减少了核β-连环蛋白水平,类似影响了hPar1-SiRNA治疗。识别PAR1下游目标/ s然而导致的形成引起公司未来的平台系统和placenta-uterus交互晚期妊娠结果的定义。

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